Eimeria nieschulzi infections in inbred and outbred rats: infective dose, route of infection, and host resistance

1973 ◽  
Vol 51 (2) ◽  
pp. 273-279 ◽  
Author(s):  
Eugene M. Liburd
Keyword(s):  
Host Resistance ◽  
Reproductive Potential ◽  
Total Resistance ◽  
Route Of Infection ◽  
Inbred Rats ◽  
Infective Dose ◽  
Eimeria Nieschulzi ◽  
Host Parasite ◽  
Dose Dependent ◽  
Mechanical Crushing

Some of the host–parasite interrelationships between Eimeria nieschulzi (Protozoa: Sporozoa) and inbred and outbred strains of rats, were analyzed. The sex of the host did not influence the severity of infection; however, starved rats as compared with fed ones produced significantly lower numbers of oocysts during an infection. Mechanical crushing of infected faeces yielded a significantly higher number of oocysts than those crushed manually. The reproductive potential of the parasite varied inversely with the dosage of oocysts. Infections were caused by parenteral injections of sporozoites through four routes. In every case these inoculations caused milder infections than those elicited by similar doses of oocysts or sporozoites given orally. All infections stimulated resistance in rats; the intensity of this immunity was dose dependent. Single doses of 2500 and 3500 oocysts or more induced total resistance in outbred and inbred rats, respectively. This immunity was demonstrated 15 days after inoculation, by challenge infections. No developing stages were found in the intestinal tissues of rats which were immunized and then challenged.

Infectivity of Trichinella isolates in mice is determined by host immune responsiveness

Parasitology ◽  
1989 ◽  
Vol 99 (1) ◽  
pp. 83-88 ◽  
Author(s):  
F. Bolas-Fernandez ◽  
D. Wakelin
Keyword(s):  
Trichinella Spiralis ◽  
Inbred Mice ◽  
Reproductive Potential ◽  
Rapid Onset ◽  
Immune Responsiveness ◽  
Parasite Relationship ◽  
Survival And Reproduction ◽  
Low Responder ◽  
Host Parasite ◽  
Dose Dependent

SUMMARYA comparison was made of the development, survival and reproduction of 5 isolates of Trichinella spiralis in inbred mice. Low responder C57BL/10 mice allowed worms of all isolates to survive longer and reproduce more successfully than did high responder NIH mice, suggesting that host immunity exerted a dominant influence upon infectivity. One isolate (Is-5 (W) — an arctic isolate) had a markedly lower infectivity than all other isolates, and was selected for more detailed study, together with isolate Is-1 (S) (a temperate isolate) which showed high infectivity. The lower infectivity of Is-5 (W) reflected a more rapid onset of immunity in mice infected with this parasite, immunity reducing the reproductive potential of female worms and causing an early expulsion from the intestine. No evidence of a dose-dependent suppression of immunity was found to explain the higher infectivity of Is-1 (S). Is-5 (W) provided a very rapid mucosal mastocytosis in infected mice, whereas Is-1 (S) caused no measurable response. In contrast, Is-1 (S) elicited higher levels of circulating parasite-specific antibodies than did Is-5 (W). These results are discussed in relation to the interplay of parasite immunogenicity and host immune responsiveness in determining infectivity, and point to the importance of identifying those immunodominant parasite molecules which control the balance of the host—parasite relationship.

shRNA targeting nonstructural protein inhibits the replication of severe fever with thrombocytopenia syndrome virus

2021 ◽  
Author(s):  
Lili Dou ◽  
Xiaoli Tao ◽  
Wei Zhao ◽  
Guofeng Zheng ◽  
Ying Lu ◽  
...  
Keyword(s):  
Tissue Culture ◽  
Western Blotting ◽  
Virus Replication ◽  
Nonstructural Protein ◽  
Vero Cells ◽  
Antiviral Effects ◽  
Infective Dose ◽  
Shrna Plasmid ◽  
Dose Dependent ◽  
Severe Fever

Aim: To explore whether shRNA targeting nonstructural protein (NSs) of severe fever with thrombocytopenia syndrome virus (SFTSV) could inhibit SFTSV replication in Vero cells. Materials & methods: SFTSV used in this experiment was propagated in Vero cells and stored at -20°C. shRNA plasmid against NSs of SFTSV was transfected to Vero cells and infected with SFTSV, after which western blotting and tissue culture infective dose (TCID50) were used to measure the virus titers. Results: shRNA against NSs protein decreased the expression of NSs and inhibited the replication of SFTSV. Conclusion: The constructed SFTSV NSs-shRNA plasmid could inhibit the replication of SFTSV. It was concluded that SFTSV NSs-shRNA could inhibit virus replication for at least 72 h. shRNA-mediated antiviral effects were dose-dependent.

scholarly journals GLUCOCORTICOIDS AND CELLULAR IMMUNITY IN VITRO

1970 ◽  
Vol 132 (6) ◽  
pp. 1055-1070 ◽  
Author(s):  
Irun R. Cohen ◽  
Lary Stavy ◽  
Michael Feldman
Keyword(s):  
Immune Reaction ◽  
Immunosuppressive Agents ◽  
Water Soluble ◽  
Embryonic Fibroblasts ◽  
Effector Phase ◽  
Inbred Rats ◽  
Sensitization Phase ◽  
Dose Dependent

We studied the influence of glucocorticoids on the sensitization phase as well as on the cytolytic effector phase of an in vitro lymphocyte-mediated immune reaction. Lymphocytes obtained from the spleens or lymph nodes of unimmunized inbred rats were sensitized against foreign rat or mouse embryonic fibroblasts in cell culture. The capacity of the sensitized lymphocytes to produce a cytolytic effect was tested by transferring them to target fibroblast cultures. Injury to target fibroblasts was measured by release of radioactive 51Cr from previously labeled fibroblasts or by direct count of viable fibroblasts after incubation with sensitized lymphocytes. Various concentrations of water-soluble hydrocortisone or prednisolone were added to cell cultures during the 5 day sensitization phase and/or during the subsequent cytolytic effector phase and the influence of these hormones on the number and cytolytic capacity of the lymphocytes was measured. During the sensitization phase, the presence of glucocorticoid hormones, at concentrations of about 1 µg/ml, led to a profound decrease in the total number of recoverable lymphocytes. However, the per cent of large transformed lymphocytes was much greater in these treated cultures. The antigen-specific cytolytic capacity per cell of the glucocorticoid-treated lymphocytes, after the hormone was removed, was several times greater than that of lymphocytes sensitized in the absence of added hormones. Glucocorticoids influenced the effector phase of the reaction by inhibiting lymphocyte-mediated injury to target fibroblasts. The hormones, at concentrations of about 1 µg/ml, inhibited the cytolytic effect by about 50% without reducing the viability of the sensitized lymphocytes. Dose-dependent toxicity to lymphocytes and increasing inhibition of cytolytic effect appeared at higher concentrations of hormones. Thus, hydrocortisone and prednisolone, at concentrations of about 1 µg/ml, did not suppress the induction of sensitization, a process which they seem to facilitate in vitro. However, similar concentrations of these hormones appear to inhibit the cytolytic effector mechanism of sensitized lymphocytes. These findings may be relevant to the use of glucocorticoids as immunosuppressive agents in vivo.

The regulation of host population growth by parasitic species

Parasitology ◽  
1978 ◽  
Vol 76 (2) ◽  
pp. 119-157 ◽  
Author(s):  
R. M. Anderson
Keyword(s):  
Population Growth ◽  
Reproductive Potential ◽  
Parasite Burden ◽  
Host Population ◽  
Parasitic Species ◽  
Regulatory Influence ◽  
Host Mortality ◽  
Parasite Reproduction ◽  
Over Dispersion ◽  
Host Parasite

SummaryThe nature of parasitism at the population level is defined in terms of the parasite's influence on the natural intrinsic growth rate of its host population. It is suggested that the influence on this rate is related to the average parasite burden/host and hence to the statistical distribution of parasites within the host population.Theoretical models of host–parasite associations are used to assess the regulatory influence of parasitic species on host population growth. Model predictions suggest that three specific groups of population processes are of particular importance: over-dispersion of parasite numbers/host, density dependence in parasite mortality or reproduction and parasite-induced host mortality that increases faster than linearly with the parasite burden. Other population mechanisms are shown to have a destabilizing influence, namely: parasite-induced reduction in host reproductive potential, direct parasite reproduction within the host and time delays in the development of transmission stages of the parasite.These regulatory and destabilizing processes are shown to be commonly observed features of natural host-parasite associations. It is argued that interactions in the real world are characterized by a degree of tension between these regulatory and destabilizing forces and that population rate parameter values in parasite life-cycles are very far from being a haphazard selection of all numerically possible values. It is suggested that evolutionary pressures in observed associations will tend to counteract a strong destabilizing force by an equally strong regulatory influence. Empirical evidence is shown to support this suggestion in, for example, associations between larval digeneans and molluscan hosts (parasite-induced reduction in host reproductive potential counteracted by tight density-dependent constraints on parasite population growth), and interactions between protozoan parasites and mammalian hosts (direct parasite reproduction counteracted by a well-developed immunological response by the host).The type of laboratory and field data required to improve our understanding of the dynamical properties of host–parasite population associations is discussed and it is suggested that quantitative measurement of rates of parasite-induced host mortality, degrees of over-dispersion, transmission rates and reproductive and mortality rates of both host and parasite would provide an important first step. The value of laboratory work in this area is demonstrated by reference to studies which highlight the regulatory influence of parasitic species on host population growth.

Recognition and polymorphism in host—parasite genetics

1994 ◽  
Vol 346 (1317) ◽  
pp. 283-293 ◽  
Keyword(s):  
Host Resistance ◽  
Restriction Enzymes ◽  
Toxin Production ◽  
Dynamical Analysis ◽  
Low Frequencies ◽  
True Nature ◽  
Evolutionary Force ◽  
Recognition Systems ◽  
Plant Pathogen Interactions ◽  
Host Parasite

Genetic specificity occurs in many host-parasite systems. Each host can recognize and resist only a subset of parasites; each parasite can grow only on particular hosts. Biochemical recognition systems determine which matching host and parasite genotypes result in resistance or disease. Recognition systems are often associated with widespread genetic polymorphism in the host and parasite populations. I describe four systems with matching host—parasite polymorphisms: plant-pathogen interactions, nuclear—cytoplasmic conflict in plants, restriction enzymes in bacterial defence against viruses, and bacterial plasmids that compete by toxin production and toxin immunity. These systems highlight several inductive problems. For example, the observed patterns of resistance and susceptibility between samples of hosts and parasites are often used to study polymorphism. The detectable polymorphism by this method may be a poor guide to the actual polymorphism and to the underlying biochemistry of host-parasite recognition. The problem of using detectable polymorphism to infer the true nature of recognition and polymorphism is exacerbated by non-equilibrium fluctuations in allele frequencies that commonly occur in host-parasite systems. Another problem is that different matching systems may lead either to low frequencies of host resistance and common parasites, or to common resistance and rare parasites. Thus low levels of host resistance or rare parasites do not imply that parasitism is an unimportant evolutionary force on host diversity. Knowledge of biochemical recognition systems and dynamical analysis of models provide a framework for analysing the widespread polymorphisms in host-parasite genetics.

scholarly journals A test of the Baldwin Effect: Differences in both constitutive expression and inducible responses to parasites underlie variation in host response to a parasite

2020 ◽  
Author(s):  
Lauren Fuess ◽  
Jesse N. Weber ◽  
Stijn den Haan ◽  
Natalie C. Steinel ◽  
Kum Chuan Shim ◽  
...  
Keyword(s):  
Gene Expression ◽  
Host Resistance ◽  
Gasterosteus Aculeatus ◽  
Constitutive Expression ◽  
Baldwin Effect ◽  
Data Set ◽  
Host Parasite Interactions ◽  
Evolution Of Resistance ◽  
Host Parasite ◽  
The Baldwin Effect

ABSTRACTDespite the significant effect of host-parasite interactions on both ecological systems and organism health, there is still limited understanding of the mechanisms driving evolution of host resistance to parasites. One model of rapid evolution, the Baldwin Effect, describes the role of plasticity in adaptation to novel conditions, and subsequent canalization of associated traits. While mostly applied in the context of environmental conditions, this theory may be relevant to the evolution of host resistance to novel parasites. Here we test the applicability of the Baldwin Effect to the evolution of resistance in a natural system using threespine stickleback fish (Gasterosteus aculeatus) and their cestode parasite Schistochephalus solidus. We leverage a large transcriptomic data set to describe the response to S. solidus infection by three different genetic crosses of stickleback, from a resistant and a tolerant population. Hosts mount a multigenic response to the parasite that is similar among host genotypes. In addition, we document extensive constitutive variation in gene expression among host genotypes. However, although many genes are both infection-induced and differentially expressed between genotypes, this overlap is not more extensive than expected by chance. We also see little evidence of canalization of infection-induced gene expression in the derived resistant population. These patterns do not support the Baldwin Effect, though they illustrate the importance of variation in both constitutive expression and induced responses to parasites. Finally, our results improve understanding of the cellular mechanisms underlying a putative resistance phenotype (fibrosis). Combined, our results highlight the importance of both constitutive and inducible variation in the evolution of resistance to parasites, and identify new target genes contributing to fibrosis. These findings advance understanding of host-parasite interactions and co-evolutionary relationships in natural systems.

Parasitism by Aphytis chrysomphali, Mercet and A. melinus Debach of Californian red scale, Aonidiella aurantoo (Maskell), in relation to seasonal availability of suitable stages of the scale

1973 ◽  
Vol 21 (1) ◽  
pp. 111 ◽  
Author(s):  
IW McLaren ◽  
GA Buchanan
Keyword(s):  
Reproductive Potential ◽  
Host Population ◽  
Early Summer ◽  
Host Parasite Relationship ◽  
Parasite Relationship ◽  
Western Victoria ◽  
Host Parasite ◽  
Relationship Of ◽  
Scale Control ◽  
North Western

A field study was undertaken to investigate the host-parasite relationship of A. aurantii and two species of Aphytis in north-western Victoria, and to suggest methods for improving and extending the biological control of A. aurantii in Victoria. Monthly samples of scale-infested Valencia oranges from five unsprayed biocontrol properties at Mildura provided information which showed a positive correlation between the percentage of available stages in the host population and the efficiency of parasitism by the Aphytis. This was thought to result from the seemingly inefficient method employed by the Aphytis in selecting a suitable host in which to oviposit; a postulate reinforced by the results of earlier work. The scarcity of suitable hosts at certain times of the year is thought to limit the efficiency of the Aphytis by reducing the chances of the parasite to achieve its reproductive potential. On the basis of this study an improved approach to red scale control is proffered, namely that attempts be made to augment the effectiveness of the established Aphytis by devising methods for increasing the proportion of available stages in red scale populations during late spring and early summer. Field and laboratory evidence indicates that parasitism by Aphytis, rather than variation in weather, is responsible for the considerable seasonal fluctuations in percentage of scales available for parasitism.

scholarly journals An alternative route of bacterial infection associated with a novel resistance locus in the Daphnia–Pasteuria host–parasite system

Heredity ◽  
2020 ◽  
Vol 125 (4) ◽  
pp. 173-183
Author(s):  
Gilberto Bento ◽  
Peter D. Fields ◽  
David Duneau ◽  
Dieter Ebert
Keyword(s):  
Host Resistance ◽  
Natural Populations ◽  
Attachment Site ◽  
Genomic Region ◽  
Infection Process ◽  
Resistance Locus ◽  
Significant Qtls ◽  
Novel Host ◽  
Trait Locus ◽  
Host Parasite

Abstract To understand the mechanisms of antagonistic coevolution, it is crucial to identify the genetics of parasite resistance. In the Daphnia magna–Pasteuria ramosa host–parasite system, the most important step of the infection process is the one in which P. ramosa spores attach to the host’s foregut. A matching-allele model (MAM) describes the host–parasite genetic interactions underlying attachment success. Here we describe a new P. ramosa genotype, P15, which, unlike previously studied genotypes, attaches to the host’s hindgut, not to its foregut. Host resistance to P15 attachment shows great diversity across natural populations. In contrast to P. ramosa genotypes that use foregut attachment, P15 shows some quantitative variation in attachment success and does not always lead to successful infections, suggesting that hindgut attachment represents a less-efficient infection mechanism than foregut attachment. Using a Quantitative Trait Locus (QTL) approach, we detect two significant QTLs in the host genome: one that co-localizes with the previously described D. magna PR locus of resistance to foregut attachment, and a second, major QTL located in an unlinked genomic region. We find no evidence of epistasis. Fine mapping reveals a genomic region, the D locus, of ~13 kb. The discovery of a second P. ramosa attachment site and of a novel host-resistance locus increases the complexity of this system, with implications for both for the coevolutionary dynamics (e.g., Red Queen and the role of recombination), and for the evolution and epidemiology of the infection process.

Host Resistance in a Natural Host-Parasite System. Resistance to Hymenolepis citelli by Peromyscus maniculatus

1973 ◽  
Vol 59 (1) ◽  
pp. 117 ◽  
Author(s):  
Donald L. Wassom ◽  
Vance M. Guss ◽  
Albert W. Grundmann
Keyword(s):  
Host Resistance ◽  
Peromyscus Maniculatus ◽  
Natural Host ◽  
Host Parasite
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